Chloroplast development is a process to resurrect photosynthesis, which powers life on the earth. The chloroplast also acts as a center of plant metabolism that biosynthesizes many important primary and secondary metabolites including amino acids, fatty acids, phytomormone precursors, vitamins and terpenoids. Thus, chloroplast functions have a broad impact on plant growth and development. Although it is well recognized that chloroplast development is regulated by coordinated expression of nuclear and plastid genes, our knowledge about regulatory mechanisms of plastid gene expression is very limited. To uncover the members involved in the process of gene expression in chloroplasts, we used leaf variegation caused by a mutation in THYLAKOID FORMATION 1 (THF1) or Psb29, an unknown protein conserved in oxygenic photosynthetic organisms, as a model system. Proteomics and genetic suppressor screening analyses showed that THF1 mutations lead to a dramatic decrease in plastid FtsH protease via an unknown mechanism. Interestingly, all suppressor lines share the common leaf virescent phenotype and have an increased level of FtsH protease. Functional analysis of these suppressor genes showed that they function in RNA processing and protein translation, suggesting that delayed chloroplast development in the suppressor lines results from defects in plastid gene expression. In addition, we also investigated the biochemical function of THF1 in regulation of photosystem II (PSII) activity. Our data showed that THF1 interacts with PSII light-harvesting complex subunits (LHCB) in a pH-dependent manner and regulates the dynamic balance between PSII mega-complex and super-complex. In summary, we infer that leaf variegation is triggered by the disrupted balance between nuclear and plastid gene expression, and is formed to protects cells from photodamage under stress.